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Artikel ; Online: Defective mitochondria remodelling in B cells leads to an aged immune response.

Iborra-Pernichi, Marta / Ruiz García, Jonathan / Velasco de la Esperanza, María / Estrada, Belén S / Bovolenta, Elena R / Cifuentes, Claudia / Prieto Carro, Cristina / González Martínez, Tamara / García-Consuegra, José / Rey-Stolle, María Fernanda / Rupérez, Francisco Javier / Guerra Rodriguez, Milagros / Argüello, Rafael J / Cogliati, Sara / Martín-Belmonte, Fernando / Martínez-Martín, Nuria

Nature communications

2024  Band 15, Heft 1, Seite(n) 2569

Abstract: The B cell response in the germinal centre (GC) reaction requires a unique bioenergetic supply. Although mitochondria are remodelled upon antigen-mediated B cell receptor stimulation, mitochondrial function in B cells is still poorly understood. To gain ... ...

Abstract The B cell response in the germinal centre (GC) reaction requires a unique bioenergetic supply. Although mitochondria are remodelled upon antigen-mediated B cell receptor stimulation, mitochondrial function in B cells is still poorly understood. To gain a better understanding of the role of mitochondria in B cell function, here we generate mice with B cell-specific deficiency in Tfam, a transcription factor necessary for mitochondrial biogenesis. Tfam conditional knock-out (KO) mice display a blockage of the GC reaction and a bias of B cell differentiation towards memory B cells and aged-related B cells, hallmarks of an aged immune response. Unexpectedly, blocked GC reaction in Tfam KO mice is not caused by defects in the bioenergetic supply but is associated with a defect in the remodelling of the lysosomal compartment in B cells. Our results may thus describe a mitochondrial function for lysosome regulation and the downstream antigen presentation in B cells during the GC reaction, the dysruption of which is manifested as an aged immune response.
Mesh-Begriff(e) Mice ; Animals ; Mitochondria/genetics ; B-Lymphocytes ; Germinal Center ; Mice, Knockout ; Lymphocyte Activation
Sprache Englisch
Erscheinungsdatum 2024-03-22
Erscheinungsland England
Dokumenttyp Journal Article
ZDB-ID 2553671-0
ISSN 2041-1723 ; 2041-1723
ISSN (online) 2041-1723
ISSN 2041-1723
DOI 10.1038/s41467-024-46763-1
Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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